Abstract
IntroductionThe purpose of our study was to determine whether hypothermia has any effects on physiological hemodynamic responses to epinephrine (Epi), and whether rewarming reverses these effects.MethodsSprague-Dawley rats were instrumented to measure mean arterial pressure (MAP), and left ventricular (LV) pressure-volume changes were recorded by using a Millar pressure-volume conductance catheter. Core temperature was reduced from 37°C to 28°C and returned to 37°C by using both internal and external heat exchangers. Two groups of rats were infused with either saline (n = 7), or Epi 0.125 μg/min continuously (n = 7). At 33°C, 30°C, and 28°C, the Epi infusion was temporarily increased from 0.125 to 1.25 μg/min.ResultsBefore cooling, Epi infusion in both groups resulted in a significant, dose-dependent increase in heart rate (HR), stroke volume (SV), cardiac output (CO), LV dP/dtmax (maximum derivative of systolic pressure over time), but only Epi infusion at 1.25 μg/min caused elevation of MAP. During cooling to 30°C, Epi infusion at 0.125 μg/min caused a significant elevation of central hemodynamic variables, whereas MAP remained unchanged. In contrast, Epi infusions at 1.25 μg/min caused a significant elevation of MAP during cooling to 28°C but no increases in central hemodynamics. After rewarming, all hemodynamic variables returned to baseline in both groups, but only the saline-treated animals displayed the prehypothermic hemodynamic dose responses to Epi infusions.ConclusionsThis study shows that hypothermia causes a change in the physiological hemodynamic response to Epi, which is not reversed by rewarming.
Highlights
The purpose of our study was to determine whether hypothermia has any effects on physiological hemodynamic responses to epinephrine (Epi), and whether rewarming reverses these effects
Baseline 37°C control values No significant differences in baseline values were found for any of the hemodynamic variables measured between saline and Epi groups at 37°C (Figures 2 and 3)
Epinephrine, 1.25 μg/min, versus saline control group Treatment with a higher dose (1.25 μg/min) of Epi infused at 37°C caused a significant (P < 0.05) increase in heart rate (HR), stroke volume (SV), cardiac output (CO), stroke work (SW), and left ventricular (LV) dP/dtmax
Summary
The purpose of our study was to determine whether hypothermia has any effects on physiological hemodynamic responses to epinephrine (Epi), and whether rewarming reverses these effects. Guidelines for using inotropic drugs to support cardiovascular function at low core temperatures are not well characterized. Such guidelines are essential for treating patients in acute heart failure, as will be the case during induced therapeutic hypothermia, as well as during rewarming from accidental hypothermia. Over the last decade, induced hypothermia is being increasingly used to reduce cerebral damage in patients after resuscitation from sudden cardiac arrest [1,2]. Rewarming shock is a clinically descriptive term that refers to a pathophysiologic state of cardiovascular collapse taking place during or after rewarming from accidental hypothermia [3]. To treat or prevent rewarming shock, cardioactive inotropic drugs are commonly necessary to elevate low CO
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